OBJECTIVE: Inflammatory responses of large vein endothelium are of importance in pathological processes such as venous thrombosis, chronic venous congestion, and vein graft atherosclerosis. However, the inflammatory properties of large vein endothelium are unclear. METHODS AND RESULTS: In this study, we used several microscopy techniques to investigate the inflammatory properties of large vein endothelium in vivo. We show that the endothelium in the mouse inferior vena cava (IVC) possesses powerful inflammatory properties that are distinct from the less inflammatory reactive aortic endothelium and virtually identical to endothelial responses in postcapillary venules. Inflammatory stimulation with tumor necrosis factor-alpha induced strong expression of cell adhesion molecules (CAMs) in the IVC. These CAMs promoted recruitment of leukocytes, platelets, and erythrocytes to the vein wall. The inflammatory responses altered endothelial structure and increased endothelial permeability in the IVC. Accumulation of blood cells and endothelial damage were markedly reduced in mice deficient in the endothelial leukocyte recruitment molecules E-selectin and P-selectin, indicating a central role for these molecules in driving structural and functional changes of IVC endothelium. CONCLUSIONS: These findings provide the first comprehensive demonstration of the inflammatory capacity of large vein endothelium and emphasize the actions of endothelial cells as targets in large vein disease.
OBJECTIVE: Inflammatory responses of large vein endothelium are of importance in pathological processes such as venous thrombosis, chronic venous congestion, and vein graft atherosclerosis. However, the inflammatory properties of large vein endothelium are unclear. METHODS AND RESULTS: In this study, we used several microscopy techniques to investigate the inflammatory properties of large vein endothelium in vivo. We show that the endothelium in the mouse inferior vena cava (IVC) possesses powerful inflammatory properties that are distinct from the less inflammatory reactive aortic endothelium and virtually identical to endothelial responses in postcapillary venules. Inflammatory stimulation with tumor necrosis factor-alpha induced strong expression of cell adhesion molecules (CAMs) in the IVC. These CAMs promoted recruitment of leukocytes, platelets, and erythrocytes to the vein wall. The inflammatory responses altered endothelial structure and increased endothelial permeability in the IVC. Accumulation of blood cells and endothelial damage were markedly reduced in mice deficient in the endothelial leukocyte recruitment molecules E-selectin and P-selectin, indicating a central role for these molecules in driving structural and functional changes of IVC endothelium. CONCLUSIONS: These findings provide the first comprehensive demonstration of the inflammatory capacity of large vein endothelium and emphasize the actions of endothelial cells as targets in large vein disease.
Authors: Andrea T Obi; Elizabeth Andraska; Yogendra Kanthi; Chase W Kessinger; Megan Elfline; Cathy Luke; Teruna J Siahaan; Farouc A Jaffer; Thomas W Wakefield; Peter K Henke Journal: Thromb Haemost Date: 2016-12-15 Impact factor: 5.249
Authors: Rohun U Palekar; Andrew P Jallouk; Matthew J Goette; Junjie Chen; Jacob W Myerson; John S Allen; Antonina Akk; Lihua Yang; Yizheng Tu; Mark J Miller; Christine T N Pham; Samuel A Wickline; Hua Pan Journal: FASEB J Date: 2015-04-09 Impact factor: 5.191
Authors: Anneleen Pletinck; Griet Glorieux; Eva Schepers; Gerald Cohen; Bertrand Gondouin; Maria Van Landschoot; Sunny Eloot; Angelique Rops; Johan Van de Voorde; An De Vriese; Johan van der Vlag; Philippe Brunet; Wim Van Biesen; Raymond Vanholder Journal: J Am Soc Nephrol Date: 2013-09-05 Impact factor: 10.121